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Fourth Year > Mammaries, Sour Grapes > Flashcards

Mammaries, Sour Grapes Flashcards

1
Q

What is mastitis?

A

Inflammation of the mammary gland with chemical and microbial changes, with increased leukocytes

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2
Q

2 types of mastitis

A

Cow associated -> source is infected mammary gland, severity depends on virulence factors

Environmental -> contamination of teat ends or intra-mammary tubes, mainly occur during drying off and in the weeks
before calving, likely to be clinical

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3
Q

3 bugs in environmental mastitis

A
  1. Streptococcus uberis (faeces,
    exotoxins)
  2. Streptococcus dysgalactiae (faeces, exotoxins)

Both strep are gram positive

  1. Escherichia coli (coliform) - gram negative, in faeces, endotoxins when killed

Others -> trueperella pyogenes, pseudomonas aeruginosa

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4
Q

4 bugs in cow associated mastitis

A

Strep agalactia (frequent - only lives in mammary gland and human skin <6d)

Strep aureus (common) - skin, can live inside WBC’s and escape antibiotics

Mycoplasma bovis - lives everywhere

Corynebacterium bovis - causes abscess, lives on skin

Staph species minor pathogen

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5
Q

Pathogenesis of mastitis

A

Organism invades udder through teat canal

Migrates up canal and colonize secretory cells

Colonized organisms produce toxic substances harmful to the milk producing cells

Immune system reaction -> somatic cells

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6
Q

How long is teat suscpetible for after milking?

A

up to 30 mins the teat remains open

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7
Q

Trigger points for action in mastitis

A

5 clinical cases per 100 cows calved

> 15DIM = More than 2 clinical cases/100 cows in milk/month

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8
Q

Post milking teat disinfection guidelines

A

Mixed fresh daily with high quality water - dont top up when low, replace it

Emollients used like glycerin (never >10%), glycan, sorbitol

0.5% iodine solution

Ensure all surfaces dipped

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9
Q

Good hygiene practices

A

Avoid milk on hands and disinfect all milk from machinery, liners, people

Milk high cell count cows last

Water for cleaning - quality (soft), temperature, concentration, quantity to be sufficient to ensure all surfaces cleaned

Good drainage in cleaning cycle - reduce microbe contamination

Maintenance of machine

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10
Q

How often should liners be changed?

A

every 2000 milkings

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11
Q

How many milkings of colostrum should be discarded from the vat?

A

first 8 milkings or 10 for induced cows

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12
Q

Data that should be monitored in dairy

A

BMCC results
Milk collection temperatures
Atypical events - water, chemicals
Errors - human or otherwise
History of milk quality

Cleaning routine specifics
Plant inspection details

Strategic milk sampling

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13
Q

Different aspects in a mastitis herd health visit

A

Farm profile
Milk cultures
ICCC
Milking machine dry time
Performance tests of machine
Clinical cases
Teat condition
Cow behaviour
Teat disinfection
The environment

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14
Q

What number of ICCC is unlikely to have subclinical mastitis? WHen is she clinically affected?

A

<150,000 cells/ml unlikely

20-100,000 is normal

> 250,000 is clinical and above 400 is unfit for human consumption

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15
Q

What is the californian mastitis test?

A

Cow-side test which is used to assess the somatic cell count of the milk for cows in all four
quarters. It can be used to test for efficacy of treatment after a bout of mastitis, or to double check a cows ICC

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16
Q

California milk test method and scoring

A
  1. Discard the foremilk
  2. 2 squirt from each quarter into the cup
  3. Add equal volume of CMT reagent
  4. Swirl and look for reaction in 8 seconds

Scoring:

0 is negative -> 0-200,000 cells and 0-25% neutrophils

T is trace (slight precipitate) -> 100-500 thousand and 30-40% neutrophils

1 is weak positive (precipitate but no gel) -> 400 to 1.5million cells and 40-60% neutrophils

2 is positive (gel) -> 800 to 5 million cells, 60-70% neutrophils

3 is strong positive (viscous gel) -> >5 million cells, 70-80% neutrophils

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17
Q

How long are californian mastitis test results valid for?

A

2h as leucocytes degenerate

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18
Q

Drying off guidelines - rate of reducing milk production + feeding

A

Dry off between 5-12L a day and reduce production to <12L a day by reducing feed intake to maintenance

Put into a clean paddock

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19
Q

Adminstering dry cow therapy guidelines

A

Identify udders of dry cows
Record cow ID, date and product

Allow for 20 cows/h

Sanitise the teat end after treatment

Minimise leakage by reducing walking and activity

Look for swollen quarters in the paddock, for heat and pain, only strip the problem quarter

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20
Q

When to cull cows with mastitis

A

Cows with 3+ clinical cases of mastitis during a lactation

A high ICCC during the previous lactation where she was dry cow treated and continued to have issues this lactation

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21
Q

Economic losses due to mastitis

A

Loss of milk production = discarded and WHP for antibiotics

Fibrosis of udder

Penalties for high SCC

Cost of vet, death in peracute cases, premature culling of cows

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22
Q

Treatment plan for peracute case of mastitis

A

IVFT - sepsis
NSAID

Tylosin - macrolide for mycoplasma, similar to erythromycin but less active against gram negatives.

Erythromycin - macrolide, lipid soluble. Good for gram positives. Resistance in mycoplasma bovis.

Trimethroprim + sulphonamide - macrolides. Not for mycoplasma. At low doses struggles to get to mammary gland. Gram negative efficacy

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23
Q

Treatment plan for acute mastitis

A

Tylosin - mycoplasma
Erythromycin - gram pos
TMS - gram negatives, multiple quarter infections

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24
Q

Chronic mastitis treatment

A

dry cow therapy

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25
Q

What is selective DCT?

A

When only cows with history of elevated ICCC or clinical mastitis get antibiotic therapy at dry off

Administered at last milking of lactation

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26
Q

How much does each clinical mastitis case cost?

A

300-400

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27
Q

What cows should samples be taken from if clinical cases are the presenting problem, or if high cell counts are the problem?

A

Clinical cases -> all cases as they are detected

high SCC -> selection for sampling based on mastitis history or recent ICCC

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28
Q

ICCC analysis purpose + unacceptable rate of new infection for heifers

What classifies a persistent infection?

A

Estimate rate of new infection in herd, get an idea of age/stage of lactation or management in all groups

Get proportion of cows above 250,000 in each group

Unacceptable rate of new infection is more than 20% of heifers being above 250,000 by end of 1st lactation

Estimate number of persistent infection -> above 250 in last and this lactation

Identify cows for foremilk stripping

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29
Q

How manny ICCC should be taken in a lactation?

A

At least 5 to get an idea of status of cow during a lactation

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30
Q

What does a california mastitis test use for reagent?

A

Alkyl arysulfonate and bromcresol purple

Lysis cells and polymerises DNA - the more gel the more DNA from nucleated cells

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31
Q

Milk fat %
Milk protein %

A

3.2-4.8 for fat

2.9-3.2 for protein

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32
Q

Milk protein to milk fat ratio

A

0.85 ideal

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33
Q

protein to fat ratio indicative of SARA

A

> 0.95

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34
Q

protein to fat ratio indicative of ketosis

A

<0.75

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35
Q

Fermentation sites in cows

A

Rumen
Caecum
Colon

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36
Q

Factors for microbial growth

A

pH close to neutral 6-7
Temp 39 degrees
Rate of flow - slow enough for multiplication of microbes

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37
Q

Major microbes

A

Bacteria
Protozoa
Fungi
Methanogens
Bacteriophages

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38
Q

Symbiotic relationship between rumen microbes and cows

A

Digestion of cellulose and hemicellulose
Provide high quality protein + B vitamins
Detoxification of toxic compounds

end product of anaerobic microbial metabolism - VFAs

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39
Q

3 VFAs and what increases them

A

Acetate -> increased with high fibre

Propionate -> increased with high starch

Butyrate -> varies with diet

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40
Q

What does accumulation of VFAs result in?

A

Decreases pH and suppresses fermentation

Host animal maintains conditions for fermentation by buffering with saliva and removing VFAs via absorption through rumen papillae

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41
Q

Sources of protein

A

True protein and non-protein nitrogen (urea)

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42
Q

Urea cycling process

A

NOn-protein nitrogen sources - nitrate, urea, ammonia

Urea is a nitrogenous waste product formed in the liver

Monogastric - excreted in kidneys

Rumen -> excreted into rumen via blood or saliva and used in protein production

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43
Q

What vitamins do bacteria make in the large intestine?

A

most of required vitamins

K and B produced by colonic bacteria

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44
Q

Non-fermentative function of large intestine

A

Absorption of water and electrolytes
Net absorption of H20, Na, Cl and bicarb and net secretion of K+

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45
Q

Aetiopathogenesis of acidosis

A

Excessively rapid fermentation of excess carbohydrate, causing a shift in VFA metabolism and a decrease in rumen pH

Accumulation of lactic acid due to lactobacillus and strep bovis which become predominant species in pH <5 = ruminal acidosis, metabolic acidosis

Saliva buffering requires enough roughage and particle size

SARA = accumulation of VFAs but not lactic acid

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46
Q

Rumenocentesis of acidotic cow

A

Milky green-brown
pH <5

47
Q

Clinical signs of ruminal acidosis

A

Anorexic, dull, ataxic, colic, tachycardic, splashing sounds, profuse water light green diarrhoea, enophthalmos, decreased feed intake

48
Q

Treatment of ruminal acidosis

A

Left flank laparotomy to remove rumen fluid
Transfaunation of rumen fluid from healthy cow
IVFT
Treat metabolic acidosis if present
Antimicrobials > procaine pen G to prevent rumenitis, bacterial hepatitis and formation of liver abscesses
Vitamin B

49
Q

Treatment of lameness

A

Hoof trimming
foot wedges to take weight off problem claw
If infected, treat

50
Q

Risk factors for lameness

A

Poor dairy enterance
rough surface
long walking distances
nutrition
wet ground

51
Q

6 major causes of lameness

A
  1. White line disease
  2. Sole injury
  3. Sole bruising
  4. Axial wall crack
  5. Footrot
  6. Digitial dermatitis
52
Q

Pathophysiology of white line disease

A

Separation of the wall from the sole
* Caused by pressure and poor cow flow leading to cows twisting and turning on hooves
* Mechanical injury from abrasive surfaces
* Wet conditions soften claw horn

53
Q

Treatment of white line disease

A
  • Pare away wall, remove underrun hoof
  • Create drainage by smoothing edges of pared area so dirt cannot pack in
  • Lift weight off affected claw by placing block/cowslip on unaffected claw
  • Treat with antibiotics or NSAIDs if required
54
Q

Sole injury pathophys

A

Sole penetration
Sole abscess
Underrun sole

55
Q

Sole injury treatment

A
  • Remove all underrun sole and any hoof wall underrun by abscess
  • Create drainage hole, but make
    sure no gravel/dirt can get trapped
  • Apply cowslip or block to unaffected claw
  • Treat with antibiotics or NSAIDs

hh

56
Q

Sole bruising at risk cows and treatment

A

first calvers

If one claw affected, apply cowslip to unaffected claw

If both claws affected, keep animal close to shed

57
Q

Axial wall crack pathophysiology

A

A crack in the inside of the claw at
the join of the hoof wall and the
sole.
* Overgrown toes
* Uneven walking surfaces
* Corkscrew claws
* Traumatic injury or disease

58
Q

Axial wall crack treatment

A

Pare underrun hoof wall in axial groove to prevent formation of proud flesh

Place cowslip or block

59
Q

Digital dermatitis pathophysiology

A
  • Infection of the digital/interdigital skin
  • Most commonly caused by
    Spirochaetes but many
    bacteria have been implicated
  • Water, mud, urine and faeces
  • Presence of bacteria

Cow to cow via environment

60
Q

Digital dermatitis treatment

A

Clean ulcer
Dry and spray with antibiotic spray (oxytetracycline) and let dry and repeat

Hygiene of herd and dairy

Good biosecurity protocol

Regular foot baths (copper sulfate)

61
Q

Footrot pathophysiology - interdigital necrobacillosus

A

Bacterial infection in
interdigital space

pungent odour, symmetrical swelling, interdigital skin necrosis

Mixed bacterial infection

62
Q

Footrot treatment

A

Investigate interdigital space

Clean the cleft and remove foreign objects or dead tissue

Spray the cleaned cleft with an
antiseptic/iodine

Check claws for other lesions

Antibiotics

63
Q

Advice for reducing lameness

A
  • Rubber laneways
  • Avoid walking cows long distances
  • Keep the dairy dry
  • Make sure the stocking density isn’t so high that the cows are standing in manure
  • Have good biosecurity to prevent digital dermatitis entering the farm
64
Q

Data required for fertility monitoring

A

Calving - dystocia, caesar, dead
Oestrus - where no serve occurs (VWP)
Service - sire, AI/natural, inseminator
Pregnancy diagnosis result
Other fertility vet exams
Metrtitis
Endometritis
Abortion

65
Q

When should fertility visits occur?

A

Every week or fortnight

66
Q

What things could deem a cow as needing action on a fertility visit?

A

Post natal checks at 21d PP
Vulval discharge
Oestrus not observed by specfic stage of lactation -> eg 24d after VWP
Pregnancy diagnosis
Repeat breeder cows
Cows overdue

67
Q

What is the herd calving index?

A

Average of calving intervals in the herd - commonly used as measure of overall performance

Useful indicator of long term performance but poor monitor when used alone -> retrospective and influenced by culling stratgey

68
Q

What does the proportion of pregnancy diagnosis that are positive tell us?

A

Detection of returns to service, and gives an idea of pregnancy rate

Should be >80% in herds where pregnancy rate is >40%

69
Q

What does the number of cycling cows presented as ONO at each visit tell us?

A

Heat detection - especially for cows due for first service

70
Q

What does calving to conception interval provide

A

Similar info to calving index but less retrospective as the end point successful service marked by pos preg test (occurs far sooner than next calving as in calving index)

71
Q

How long is pregnancy

A

280d

72
Q

What does submission for service encompass?

A

Oestrus expression and detection as well as post partum return to cyclicity

73
Q

What is the first service submission rate?

A

Proportion of cows receiving first service within 24d of becoming eligible (eg after VWP)

Most cows should have oestrus within 24d of VWP

74
Q

What is the return to service submission rate?

A

proportion of failed serves (not leading to preg) which a subsequent serve occurs 18-24d later

Should be lower than first service submission rate

75
Q

What is clinical metritis characterised by?

A

Purulent uterine discharge with abnormally enlarged uteris within 21d calving but no other clinical signs

76
Q

Factors affecting oestrus expressoin

A

Lameness
Pain
Stress
Mastitis
High yielding cows - express for less time or less intensely
Non-slip, squishy floors - help
Prefer outdoor loafing for oestrus behaviour rather than inside
Time spent in milking -> 3x a day, less time for oestrus more time in holding yards

77
Q

How much loafing area is required for each cow?

A

2-3m2 per cow minimum

78
Q

How does NEB affect pregnancy rate?

A

Risk factor for retained fetal membranes, metritis, ketosis, disaplced abomasum

Low IGF-1 -> decreased response of ovary to gonadotropins

79
Q

When should cows be AI’d after showing first signs of oestrus?

A

No later than 10-12 hours later

80
Q

Organisms and diseases spread through reproduction

A

Tritrichomonas fetus
Campylobacteriosis
Mycoplasma
Ureaplasma
IBR
BVDV

81
Q

Acquiring mastitis samples

A

Good aseptic technique - wash and dry teats well with disinfectant, squirt 6 times and repeat
Immediately fridge or freeze
Pre-milking are more diagnostic than post milking

label tube with cow id, quarter, date

82
Q

For every 100,000 cell/ml increase in BMCC, how many cows are infected?

A

8-10% increase in proportion of cows infected in the herd

83
Q

Aims when attempting to control mastitis

A

Reduce prevalence of infection - number and duration of existing infection, as well as new infection

Cull chronic cows
Best chance to cure chronic cows is in the dry period

Decifer if its environmental or contagious

84
Q

Mastitis investigation approach

A
  1. establish goals and herd targets
  2. Assess current practice and find deficiencies
  3. Evaluate data - SCC and clinical mastitis data from at least past 18 months to detect patterns of disease
  4. Determine source of infection and control measures
  5. Monitor outcomes
85
Q

3 ways to reduce herd prevalence of mastitis infection

A

Dry off infected quarters
cull
treat

86
Q

Things associated with poorer prognosis of cure in mastiis

A

Chronic high cell count
Severe teat lesions
Other health problems
Delay in initiation of treatment
Increasing parity
more than 1 quarter affected
Beta-lactamase producing s.aureus
Fibrosis of mammary gland

87
Q

Define lameness

A

The clinical presentation of impaired locomotion

88
Q

Where does most lameness occur?

A

Hind feet
Mostly due to claw lesions with remainder being limb lesions

89
Q

4 causes of lameness

A

Sole ulcer
White line disease
Digital dermatitis
Interdigital necrobacillosis

90
Q

Economic losses of lameness

A

Infertility - anoestrus or not wanting to stand
Culling
Reduction in milk yield
Treatment costs
Professional fees

91
Q

Lameness scale 1-5

A
  1. Stands and walks with a level back posture; gait is normal
    2 Stands with level back but arched back when walking; gait is normal
    3 Arches back when walking and standing; gait is affected
    4 Arched back posture always evident; gait shows deliberate steps
    5 Inability or extreme reluctance to bear weight on one or more limbs
92
Q

Mobility index industry benchmark

A

90%

93
Q

Industry benchmark values for lameness score 4 and 5

A

0.5% for both

94
Q

How often should locomotion scoring occur? What should it be concurrent with?

A

every 2-4wks to detect subclinical and clinical lameness

Routine evaluation of claw health, hoof trimming and abnormality detection

95
Q

Why is BMCC useful to monitor herd mastitis?

A

Daily updates
Indirect measure of subclinical in herd - approximate infection level
Easy access to information
Sudden increase suggests a clinical case is present

96
Q

Benchmark for 3-5 lameness score

A

10%

97
Q

TCM period

A

3 weeks prior to 4 weeks post calving

98
Q

Does DMI decrease around calving?

A

Yes by 30% - and more so in cows in high BCS

99
Q

Which cows are more at risk of lameness?

A

Cows with poor BCS at calving and lactation
BCS is positively correlated with thickness of digital cushion

100
Q

Methods to reduce lameness

A

Feed pregnant heifers a high dry matter diet and limit BCS loss prior to calving

101
Q

What decreases with SARA?

A

Milk fat
Rumen pH -> less than 5.5 is clinical

102
Q

SARA MOA

A

Excessive fermentation of sugars and starches with inadequate fibre and buffering of the rumen

Poor TCM, feeding high fermentable food, high starch, low fibre, excess finely ground particles

103
Q

Ketosis NEFA cutoffs 2 weeks and 1 week prior to calving

A

NEFA increases prior to calving anyway

1 weeks prior = <0.6mmol/L (any more is a risk)

2 weeks prior = <0.3mmol/l is appropriate

104
Q

Type 1 ketosis is:

A

where nutritional demands after calving are not met
3-6 weeks post calving
Bad yields and poor fertility

105
Q

Type II ketosis is:

A

Associated with fatty infiltration of the liver
Elevated NEFA immediately post calving
BHB’s elevated 5d post calving

106
Q

Collecting samples for ketosis

A

Tail/jugular
Will increase with haemolysis so separate within few hours and freeze/chill

107
Q

Reasons for buffering failure

A

Not ruminating or chewing new food
Inadequate fibre length (5-10cm) - to form fibre mat in rumen to trap in food for microbial digestion

Feeding high fermentable foods
Poor cow comfort - less lying/ruminating time

108
Q

What increases acetate?

A

Structural carbohydresa (cellulose, hemicellulose)

Need acetate to make milk fat

109
Q

What increases proprionate?

A

Non-structural carbohydrates

110
Q

What VFA does milk fat rely on?

A

Acetate

111
Q

What do VFA’s do in SARA?

A

Propionate (from non-structural carb) = increases

Acetate = decreases = less milk fat

112
Q

Prevalence of lameness score 2 for a cause of investigation

A

More than 5% prevalence of lameness score 2 cows is cause to investigate acidosis as a possible factor in a lameness problem

113
Q

Targets for ketosis, hypocal, clinical mastitis and lameness in the herd

A

<3-5% ketosis and hypocal in the herd
<2-5% clinical mastitis cases a month
<5% lameness (<10% claw abnormalities)

114
Q
A

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